Mechanism of inflammation and death
Key Protein Found to Trigger Inflammation and Cell Death
Svetlana Maslova, Hi-tech+
The discovery is of great importance for understanding previously unknown functions of the immune system. Now scientists know under what conditions interleukin-1a matures and is released, which is an important part of triggering the immune response.
Article by Tsuchiya et al. Gasdermin D mediates the maturation and release of IL-1α downstream of inflammasomes published in Journal:Cell Reports – VM.
Japanese scientists from Kanazawa University sought to find out what contributes to the maturation and release of interleukin-1a during the activation of inflammasomes – participants in the innate immune system that trigger an inflammatory response. This mechanism is very important for a deeper understanding of the nature of inflammatory diseases and immune system responses to viruses and other pathogens.
From previous studies, scientists knew that the protein gazdermine D could be an important player in this process, but until now they could not determine its effect on interleukin-1α (IL-1α). Earlier, they found out that the activation of inflammasomes leads to the separation of gasdermin D into two parts. One of them promotes the formation of membrane pores, which later lead to cell death.
Now they have removed the gene encoding gasdermine D and found that this almost completely disrupts the release of IL-1α from cells. In addition, there were no mature IL-1a either. "This made us think that this protein is important not only for the release, but also for the maturation of IL-1a," said co–author Takashi Suda.
Further experiments confirmed their hypothesis. It turned out that the formation of pores with the help of gazdermine D provides an influx of calcium and activation of calpain enzymes, which as a result converts the precursors into mature IL-1a.
"The identification of gazdermin D as a regulator of immune function and cell death improves our understanding of how the inflammasome ultimately leads to the release of IL-1a," the authors concluded.
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